Toll-like receptor is expressed by various immune cells and recognizes high reserved structural motifs: Pathogen Associated Molecular Pattern (PAMP) expressed by microorganism pathogens or Damage Associated Molecular Patterns (DAMP) released by dead cells. PAMP or DAMP stimulates Toll-like receptor to trigger signal cascade which induces the activations of transcriptional factors like AP-1, NF-κB and interferon regulators (pulse response function). It results in various cell responses, including productions of interferons, proinflammatory cytokines and effector cytokines, whereby immune response is produced. By far, 13 types of Toll-like receptors have been discovered. Toll-like receptors 1, 2, 4, 5 and 6 are mainly expressed on the cell surface while Toll-like receptors 3, 7, 8 and 9 are expressed in the endosome. Different Toll-like receptors recognize ligands derived from different pathogens. Toll-like receptor 7 (TLR7) is expressed and ligand recognized by plasmaeytoid dendritic cells (pDC) to induce the secretion of interferon α (IFN-α). Toll-like receptor 7 (TLR7) and Toll-like receptor 8 (TLR8) are highly homologous and therefore the ligand of TLR7 in most cases is also that of TLR8. TLR8 stimulation mainly induces the productions of cytokines like tumor necrosis factor α (TNF-α) and chemoattractant. Interferon α is one of the medicines for treating chronic hepatitis B or hepatitis C while TNF-α is a proinflammatory cytokine, of which the over secretion will result severe side effects. Therefore, the selectivity for TLR7 and TLR8 is important for the development of TLR7 agonist for treating virus infective diseases. There have been reported several TLR7 agonists, like imiquimod, resiquimod, GS-9620. Nevertheless, it is desirable to have novel TLR7 agonists with better selectivity, activity and safety. We have identified a series of novel pyrrolopyrimidine derivates as TLR7 agonist. The background of our research may be found at the following journals: Hoffmann, J. A., Nature, 2003, 426, p 33-38; Akira, S., Takeda, K., and Kaisho, T., Annual. Rev. Immunology, 2003, 21, 335-376; Ulevitch, R. J., Nature Reviews: Immunology, 2004, 4, 512-520; Coffman, R. L., Nat. Med. 2007, 13, 552-559; Paul A. Roethle, J. Med. Chem. 2013, 56(18), 7324-7333.